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K Yoshimura

Publications and source records attributed to K Yoshimura.

At least 487 records · Page 27Linked to original sources
PubMed1986

Selective IgA deficiency in Japanese blood donors: frequency and statistical analysis.

The incidence of selective IgA deficiency (SIgAD) was determined in a healthy adult population of 222,597 Japanese volunteer blood donors. Of the blood donors screened, only 0.007% (1:14,840) were found to be IgA-deficient (less than 10 mg/dl) by means of the double diffusion method, while 0.005% (1:18,500) were less than 5 mg/dl, and 0.003% (1:31,800) were less than 1 mg/dl by means of the single radial immunodiffusion method. Statistical analysis of the results clearly showed that the incidence of SIgAD in Japanese blood donors is very much lower than that in blood donors of European ancestry. The Japanese population may occupy a unique position in the ethnical peculiarities. Anti-IgA antibodies were found in 3 (25.0%) of 12 IgA-deficient blood donors whose IgA levels were less than 5 mg/dl, a prevalence rate comparable to that in donors of European ancestry. Although it is difficult to develop a suitable file of IgA-deficient donors in Japan, the establishment of a Rare Donor Registry System on IgA deficiency is a matter of urgency.

Adolescent↗
PubMed1986

Changes in intracellular K+ and Na+ ion concentrations during cell growth and differentiation.

We compared intracellular K+ and Na+ ion concentrations during cell growth and differentiation of a mouse myeloid leukemia M1 cell line. Cells undergoing mitosis had higher K+ concentrations than quiescent cells. Treatment with a K+ channel blocker and furosemide enhanced cell growth and produced a slight increase in the intracellular K+ concentration. Treatment with reagents that reduced the intracellular K+ concentration stopped cell growth. Induction of differentiation in this cell line produced a decrease in the K+ concentration, which always was accompanied by an increase in the Na+ concentration. Treatment with ouabain, which decreased the intracellular K+ concentration, did not, however, induce differentiation in the M1 cell line. The data suggest that cell growth and differentiation in the M1 cells are accompanied by changes in the intracellular K+ and Na+ concentrations but that the changes in the contents of these monovalent cations do not necessarily induce differentiation in this cell line.

Animals↗
PubMed1986

Continuous, low dose of hydralazine, reduces acute hypoxic pulmonary hypertension without a corresponding fall in systemic arterial pressure.

Administration of hydralazine in patients with pulmonary hypertension has been reported to cause excessive systemic vasodilatation, limiting its clinical utility (N Engl J Med 1982; 306: 1326). We studied the effects of hydralazine on hypoxic pulmonary vasoconstriction (HPV) in chronically instrumented sheep and evaluated whether different methods of intravenous administration could prevent severe systemic hypotension. Mean left atrial, pulmonary and systemic arterial pressures (Pla, Ppa and Psa mmHg), cardiac output (CO, l/min, electromagnetic flowmeter) and heart rate were measured continuously. Systemic (SVR) and pulmonary vascular resistances (PVR) were calculated by Psa/CO and (Ppa-Pla)/CO, respectively. Following a 30 min baseline period, we initiated hypoxia with mixture of 10% oxygen in nitrogen. After 20 min of hypoxia we then performed the following two experiments: Group A-Hydralazine (10 micrograms/kg/min) was infused continuously for a further 20 min of hypoxia (n = 6); Group B-Hydralazine (400 micrograms/kg) was administered as a single bolus, followed by an additional 20 min of hypoxia (n = 6). In both Groups A and B, hypoxia produced a prominent pulmonary hypertensive response. Continuous infusion of hydralazine (Group A) significantly decreased the hypoxic values of Ppa and PVR from 25.1 +/- 1.1 to 21.7 +/- 1.6 mmHg (p less than 0.01) and from 4.82 +/- 0.50 to 4.17 +/- 0.40 mmHg/l/min (p less than 0.05), respectively. In Group B, hydralazine as a bolus also significantly decreased HPV, with Ppa dropping from 20.9 +/- 0.9 to 18.3 +/- 1.5 mmHg (p less than 0.05) and PVR falling from 4.98 +/- 0.55 to 4.34 +/- 0.53 mmHg/l/min (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

[Immunohistochemical studies of fetal and maternal endocrine pancreases during pregnancy and the puerperium in streptozotocin-induced diabetic rats].

In order to clarify the influence of the diabetic state on the structure of maternal and fetal endocrine pancreases, the distribution of alpha, beta and delta cells in the islets of Langerhans (IL) was investigated by PAP methods in normal and streptozotocin (STZ)-induced diabetic rats. The size of the IL significantly increased during pregnancy and on day 14 of puerperium in normal and diabetic maternal rats. The total cell numbers of IL also increased during pregnancy but decreased in puerperium in both groups. Although the number of beta cells was reduced in STZ-treated rats, they could increase during pregnancy as in the normal group. The number of beta cells kept increasing in puerperium in the diabetic group, but not in the normal group. The number of alpha and delta cells in diabetic rats was greater than in normal rats but did not change remarkably during pregnancy and in puerperium. The IL of fetuses from diabetic mothers were slightly greater in size and number than those from normal mothers. The number of fetal beta cells from normal mothers was somewhat greater than that from diabetic mothers. The number of fetal alpha and delta cells from diabetic mothers was slightly greater than that from normal mothers. These findings, therefore, suggest that diabetic IL could adapt themselves to pregnancy-induced metabolic changes.

Animals↗
PubMed1986

[Three-dimensional analysis of colonic adenoma and of carcinoma in adenoma with scanning electron microscope and sequential serial sectioning].

Three-dimensional structures were analyzed on 32 human colonic adenomas, 5 hyperplastic polyps, 4 normal colonic mucosa and 5 advanced colonic carcinomas with Scanning Electron Microscope (SEM) and with sequential serial sectioning. After SEM observation, the samples were softened with 2% NaHCO3 and observed with histological serial sectioning. By combining both techniques, that is combined analysis of outer structures for SEM and inner structures for serial sectioning, three dimensional analysis of the colonic adenoma and carcinoma in adenoma were successfully completed. The colonic adenomas were classified into 6 types based on the surface structure observed by SEM as Type I (circular type), Type II (long-elliptical type), Type III (branched type), Type IV (gyral type), Type V (wrinkle type) and Type VI (complicated type). Classified Types I, II, III and IV were observed in tubular adenoma, and grades of atypia seemed to be increased as increasing type numbers. Type V, in tubulo-villous adenoma and villous adenoma, were found out and showed severer atypia than observed in Type IV. Among 32 adenomas, 3 portions of focal cancers were detected, and the surface structures of them had highly complicated patterns as shown with Type VI.

Adenoma↗
PubMed1986

[Studies on somatomedin C in diabetic pregnancies].

Somatomedins have been shown to have potent mitogenic activities in cultured cells and also promote individual growth. We studied the concentrations of somatomedin C in diabetic pregnant women and rats. Serum and liver somatomedin C were measured by RIA double antibody method, after extraction with an ODS silica column. Serum somatomedin C concentrations were 20.45 +/- 5.14 nM/l (mean +/- S.D.) in nonpregnant normal women. In nonpregnant diabetic women, these were 16.96 +/- 4.37 nM/l, which were significantly lower than those of normal nonpregnant women. The concentrations of pregnant normal and diabetic women were similar to those of nonpregnant normal women. Maternal concentrations of somatomedin C significantly correlated with infant weight (r = 0.41, p less than 0.05, n = 41). Serum somatomedin C concentrations in the normal infants were 6.45 +/- 1.97 nM/l, which were considerably lower than those of their mothers. In the infants from diabetic mothers, these were 9.17 +/- 3.28 nM/l, which were significantly higher than those of normal infants. Rat serum somatomedin C concentrations which were 15.86 +/- 2.37 nM/l in nonpregnant normal rats, tended to increase during pregnancy. The mother's concentration significantly correlated with fetus weight (r = 0.491). Liver somatomedin C levels decreased in diabetic and pregnant states. Fetal rats had lower hepatic somatomedin C, which was about 10% of the mother's levels. These were higher in the fetuses from diabetic mothers. These finding suggested that the mother's somatomedins might contribute to fetal growth.

Animals↗